Nature Genetics
- 33, 328 - 330 (2003)
doi:10.1038/ng0303-328
Intoxicated cells and stomach ulcersRichard M. Peek Jr.
Division of Gastroenterology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA and Department of Veterans Affairs Medical Center, Nashville, Tennessee 37212, USA. richard.peek@vanderbilt.edu
Helicobacter pylori induces chronic gastritis in virtually all hosts, yet only a fraction of colonized patients ever develop peptic ulcer disease. A new study shows that binding of the H. pylori virulence determinant VacA by a receptor tyrosine phosphatase, Ptprz, modifies the phosphorylation pattern of gastric epithelial cell proteins and leads to cellular detachment. As activation of Ptprz also results in gastric injury and ulceration in vivo, these findings help explain why VacA-expressing strains of H. pylori augment the risk for peptic ulcer disease
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